We have shown that in the distal photoreceptors of the scallop eye, light activates rhodopsin, which leads to an increase in K ion permeability (Pk) of its membrane and results in a hyperpolarizing receptor potential. Treatment of the photoreceptor with 3 times normal external Ca2 ion to promote a greater Ca2 ion influx and therefore a higher intracellular Ca2 ion concentration (Cai) hyperpolarizes the dark membrane potential, following a brief period of depolarization, and reduces or eliminates the photoreceptor potential. Similarly, treatment with agents, such as DNP or cyanide, which inhibit the mitochondrial uptake of free internal Ca2 ion and therefore also increase Cai, has the same effect. The dark membrane potential hyperpolarization is due to an increase in PK. Conversely, inhibition of Ca2 ion movement by the addition of 10 mM Co2 ion or Mn2 ion to the external medium depolarizes the dark membrane potential and produces a decrease in membrane conductance. During this period the receptor potential amplitude is decreased. Our results suggest that the light induced increase in PK and the resulting hyperpolarizing receptor potential of these cells is mediated by an increase in Ca.